**10. Cytokines and SLE**

IL-10 is a pivotal cytokine which inhibits T cells and antigen-presenting cells while enhancing B-cell survival and activity. IL-1β, IL-10 and TNF-a genes are important in the pathogenesis of SLE. It has been found that ILβ-511, IL-1β + 3953, IL-10-1082 and TNF-a-308 polymorphisms may be linked to the risk of lupus development and also to a specific phenotype. The high TNF alpha genotypes - 308AA - were associated with SLE independently of IL10 alleles, but the risk of developing CCLE and the prevalence of discoid lesion phenotype - in SLE - were higher in the high IL10/ low TNF alpha producer group (−1082/−308GG). In addition, interaction between different cytokines modifies the appearance of autoantibodies. Patients who produce low levels of both TNF alpha and IL10 present anti-Sm-antibodies while patients who produce low IL10/high TNF alpha present more frequently antibodies to SSa and SSb.

Furthermore, interleukin 23R gene polymorphisms especially the IL23Rrs10889677 confers SLE susceptibility to individuals of certain ethnicities, such as IL17 A haplotype polymorphisms. In addition, Interleukin-1 receptor antagonist gene polymorphism is a disease severity factor in SLE [21–24].
